Differences Between Changes in Serum Thyrotropin-Binding Inhibitory Antibodies and Thyroid-Stimulating Antibodies in the Course of Antithyroid Drug Therapy for Graves' Disease

Abstract

There has recently been controversy regarding whether the measurement of thyrotropin-binding inhibitory antibodies (TBIAb) is useful in the management of Graves' disease. Another method of assessing Graves' disease by measuring adenylate cyclase activity in thyroid cells, known as thyroid-stimulating antibodies (TSAb), differs from TBIAb not only in terms of assay but also in immunoglobulin type according to recent studies. In this study, the concentrations of TBIAb and TSAb were compared in serial serum samples collected from 29 patients with Graves' hyperthyroidism during 12 months of antithyroid drug therapy. Before therapy, there was a correlation between TBIAb and TSAb (r = 0.59). The radioactive iodine uptake (RAIU) was not significantly correlated with either TBIAb or TSAb (r = 0.20 and r = 0.29, respectively), and the serum free thyroxine (FT4) concentration was also not significantly correlated with either TBIAb or TSAb (r = 0.06 and r = 0.22, respectively). In patients with Graves' ophthalmopathy, TSAb levels were higher than in patients without ophthalmopathy (1015%+/-851% vs. 456%+/-323%, p<0.01), but the TBIAb levels were not significantly different. After antithyroid treatment, TBIAb did not decrease significantly (from 42.1%+/-20.8% to 20.5%+/-19.5%, p = 0.29). On the other hand, TSAb was significantly decreased after 12 months of treatment (from 649%+/-611% to 294%+/-205%, p< 0.05). These findings indicate that TBIAb and TSAb are not identical, and that TSAb has a closer relationship to thyroid function than TBIAb. In the clinical setting, determination of the serum TSAb level may provide a more accurate index of the thyroid status in Graves' disease patients receiving antithyroid therapy.

Prediction of Remission or Relapse for Graves’ Hyperthyroidism by the Combined Determination of Stimulating, Blocking and Binding TSH-Receptor Antibodies after the Withdrawal of Antithyroid Drug Treatment

“…These results are in accordance with reports describing TRAbs that bind but do not stimulate the TSH receptor [20,21]. Furthermore, differences between changes in TBII and TSAbs were identified during and after ATDT [22]. Therefore, the prediction of the individual course of GD after ATDT can most likely only be improved by a repeated and combined highly sensitive determination of hTBII, TSAbs and TSBAbs after the withdrawal of ATDT.…”

“…This can most likely be explained by the combination of significant TSAb changes and the changes of different TRAb qualities that do not need occur together during the course of GD in our patients (Fig. 2 a) and reported by others [22] respectively.…”

“…The determination of TSAbs (OR = 26; p = 0.01) showed a significantly higher prognostic value for relapse than hTBII (OR = 4; p = 0.1) or TSBAB (OR = 8; p = 0.03) respectively ( Table 2). The higher prognostic value of the TRAb determination at time x compared to the end of ATDT, especially for the TSAB determination, is most likely due to the previously reported changes of TRAb during the course of GD [13,22,26] and the significant changes of the TSAB activity in those patients who achieved remission after the end of ATDT in our study.…”

“…Furthermore, it has been demonstrated that the determination of TRAbs prior to or Prediction of Remission or Relapse for Graves' Hyperthyroidism by the Combined Determination of Stimulating, Blocking and Binding TSH-Receptor Antibodies after the Withdrawal of Antithyroid Drug Treatment at the beginning of ATDT has no prognostic value in predicting Graves hyperthyroidism relapse [7,12]. Moreover, TBII and TSAb courses during ATDT vary [22]. Therefore, TRAb values determined before ATDT are not useful in predicting remission or relapse after ATDT.…”

Induction of TSH-Receptor Antibodies in Patients with Toxic Multinodular Goitre by Radioiodine Treatment

“…The only difference between the previously investigated patients with TMG type A and the present cohort of patients is the methimazole treatment. Therefore, the discrepancies between detectable TBII and TSAB-or TSBABactivity can most likely be explained by the methimazole treatment as suggested in a previous study on patients with GD [21]. This explanation is supported by a previous investigation that showed a higher frequency of TBII positivity in patients with DISA without antithyroid drug treatment (39 % versus 11 %) compared to those who had not received any treatment [11].…”